The discovery of cycasin, methylazoxymethanol (MAM), 1,2- dimethylhydrazine (DMH), and azoxymethane (AOM), as agents which produce colon tumors in experimental animals is relatively recent and the metabolic fates of these compounds are not well understood. It appears that DMH and AOM are not carcinogenic in themselves but are converted to active carcinogens in animal tissues. It has been postulated that DMH and AOM are oxidized to MAM in the liver, conjugated as the glucuronide, and excreted with the bile. The MAM-glucuronide is transported to the colon and it is assumed to be hydrolyzed by the Beta-glucuronidase produced by the microflora to release free MAM, the proximate carcinogen. This project seeks to determine whether or not DMH and AOM are converted to MAM in accord with the postulate, or are transformed to methylating agents by other metabolic pathways; established the presence or absence of an enterohepatic excretion cycle; and to evaluate the relative importance of intestinal microflora and tissue enzymes in the chemical colon carcinogenesis of these compounds.